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感觉纤维在吉兰-巴雷综合征轴索亚型中的作用。

Involvement of sensory fibres in axonal subtypes of Guillain-Barre syndrome.

机构信息

Department of Neuroscience and Imaging, University G d'Annunzio, Chieti-Pescara, Italy.

出版信息

J Neurol Neurosurg Psychiatry. 2011 Jun;82(6):664-70. doi: 10.1136/jnnp.2010.238311. Epub 2011 Mar 28.

Abstract

BACKGROUND

Acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN) are due to an antiganglioside antibody mediated attack, thought to be restricted to motor fibres in AMAN. Sensory symptoms and minor sensory conduction abnormalities, however, have been reported in some AMAN patients.

OBJECTIVE

To verify whether sensory fibres are truly spared in AMAN and whether AMAN and AMSAN represent a continuum.

METHODS

Serial conduction studies in 13 AMAN and three AMSAN patients were reviewed. To evaluate the variation in sensory nerve action potential (SNAP) amplitude in serial recordings, the least significant change in a test-retest study of 20 controls was calculated. Least significant change for median, ulnar and sural nerves were 44%, 47% and 58%, respectively.

RESULTS

In 34% of initially normal sensory nerves of six AMAN patients, SNAP amplitude significantly increased by 57-518%. In three nerves of three AMAN patients, SNAP significantly decreased by 50-69%. Overall, serial recordings allowed detection of sensory fibre involvement in 49% of nerves and in 69% of AMAN patients. In one AMSAN patient, SNAP increased in two nerves by 150-300%; in another patient, SNAPs, unrecordable at baseline in six nerves, reappeared during follow-up and normalised in three nerves. In five nerves of three AMAN and in eight nerves of two AMSAN patients, SNAP amplitudes increased rapidly, suggesting reversible conduction failure of sensory fibres. In other nerves, SNAP increased over months, as for axonal regeneration.

CONCLUSIONS

Sensory fibres are often involved subclinically in AMAN. Reversible conduction failure may develop in sensory as well as motor fibres in both AMAN and AMSAN. AMAN and AMSAN represent a continuum in axonal GBS.

摘要

背景

急性运动轴索性神经病(AMAN)和急性运动感觉轴索性神经病(AMSAN)是由抗神经节苷脂抗体介导的攻击引起的,据认为这种攻击仅限于 AMAN 中的运动纤维。然而,一些 AMAN 患者报告了感觉症状和轻微的感觉传导异常。

目的

验证 AMAN 中感觉纤维是否真的未受累,以及 AMAN 和 AMSAN 是否代表一个连续体。

方法

对 13 例 AMAN 和 3 例 AMSAN 患者的系列传导研究进行了回顾。为了评估连续记录中感觉神经动作电位(SNAP)幅度的变化,计算了 20 例对照者的测试-再测试研究中的最小有意义变化。正中神经、尺神经和腓肠神经的最小有意义变化分别为 44%、47%和 58%。

结果

在 6 例 AMAN 患者的最初正常感觉神经中,有 34%的 SNAP 幅度显著增加了 57%-518%。在 3 例 AMAN 患者的 3 根神经中,SNAP 显著降低了 50%-69%。总的来说,连续记录在 49%的神经和 69%的 AMAN 患者中检测到了感觉纤维受累。在 1 例 AMSAN 患者中,2 根神经的 SNAP 增加了 150%-300%;在另 1 例患者中,6 根神经在基线时无法记录到 SNAP,在随访期间再次出现,并在 3 根神经中恢复正常。在 3 例 AMAN 的 5 根神经和 2 例 AMSAN 的 8 根神经中,SNAP 幅度迅速增加,提示感觉纤维的可逆传导失败。在其他神经中,SNAP 在数月内增加,这是轴索性吉兰-巴雷综合征的再生过程。

结论

感觉纤维在 AMAN 中经常亚临床受累。感觉纤维和运动纤维在 AMAN 和 AMSAN 中都可能发生可逆的传导失败。AMAN 和 AMSAN 在轴索性吉兰-巴雷综合征中是一个连续体。

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